Bisphenol A (BPA) is a ubiquitous component in the manufacturing of plastic. It is commonly found in food and beverage containers. Because of its broad exposure and evidence that it may act as an estrogen-like molecule, many have studied its potential effects. For example, epidemiological studies have found an association between in utero BPA exposure and onset of childhood asthma. Our previous work suggested BPA treated mice induced asthma-like symptoms in both mothers and their pups. In order to better understand theconsequences of BPA exposure and potential mechanisms, we used a proteomics approach. Using both CD4 T cells from an in vivo model of BPA exposure and an in vitro epithelial cell model, we identified activation of both innate and adaptive immune signaling following BPA exposure. Furthermore, our proteomic results from our multigenerational mouse model study implicates aberrant immune activation across several generations. We propose the following; BPA can active an innate viral immune response by upregulating a probable palmitoyltransferase ZDHHC1, and its binding partner stimulator of interferon-gamma (STING). It also has additional histone epigenetic perturbations, suggesting a role for epigenetic inheritance of these immune perturbations.
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http://dx.doi.org/10.1021/acs.jproteome.9b00548 | DOI Listing |
Viruses
January 2025
Center for Virus-Host-Innate-Immunity, Institute for Infectious and Inflammatory Diseases, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ 07103, USA.
The type I interferon (IFN-I) response is a critical component of the immune defense against various viral pathogens, triggering the expression of hundreds of interferon-stimulated genes (ISGs). These ISGs encode proteins with diverse antiviral functions, targeting various stages of viral replication and restricting infection spread. Beyond their antiviral functions, ISGs and associated immune metabolites have emerged as promising broad-spectrum biomarkers that can differentiate viral infections from other conditions.
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January 2025
Institute of Virology, Department of Infectious Diseases, University of Veterinary Medicine Hannover, D-30559 Hannover, Germany.
The first marine pestivirus, Phocoena pestivirus (PhoPeV), isolated from harbor porpoise, has been recently described. To further characterize this unique pestivirus, its host cell tropism and growth kinetics were determined in different cell lines. In addition, the interaction of PhoPeV with innate immunity in porcine epithelial cells and the role of selected cellular factors involved in the viral entry and RNA replication of PhoPeV were investigated in comparison to closely and distantly related pestiviruses.
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January 2025
Department of Veterinary Prevention and Avian Diseases, Faculty of Veterinary Medicine, University of Life Sciences in Lublin, 20-033 Lublin, Poland.
Bacteriophages, as ubiquitous bacterial viruses in various natural ecosystems, play an important role in maintaining the homeostasis of the natural microbiota. For many years, bacteriophages were not believed to act on eukaryotic cells; however, recent studies have confirmed their ability to affect eukaryotic cells and interact with the host immune system. Due to their complex protein structure, phages can also directly or indirectly modulate immune processes, including innate immunity, by modulating phagocytosis and cytokine reactions, as well as acquired immunity, by producing antibodies and activating effector cells.
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January 2025
Department of Microbiology, Immunology and Transplantation, Rega Institute, KU Leuven, Herestraat 49, 3000 Leuven, Belgium.
The Rift Valley fever virus (RVFV) causes haemorrhagic fever, encephalitis, and permanent blindness and has been listed by the WHO as a priority pathogen. To study RVFV pathogenesis and identify small-molecule antivirals, we established a novel In Vivo model using zebrafish larvae. Pericardial injection of RVFV resulted in ~4 log viral RNA copies/larva, which was inhibited by the antiviral 2'-fluoro-2'-deoxycytidine.
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January 2025
Department of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
The tripartite-motif protein 56 (TRIM56) is a RING-type E3 ubiquitin ligase whose functions were recently beginning to be unveiled. While the physiological role(s) of TRIM56 remains unclear, emerging evidence suggests this protein participates in host innate defense mechanisms that guard against viral infections. Interestingly, TRIM56 has been shown to pose a barrier to viruses of distinct families by utilizing its different domains.
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